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Emerging Pharmacotherapy to Reduce Elevated Lipoprotein(a) Plasma Levels
Author(s) -
Nathaniel Eraikhuemen,
Dovena Lazaridis,
Matthew Dutton
Publication year - 2020
Publication title -
american journal of cardiovascular drugs
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.063
H-Index - 50
eISSN - 1179-187X
pISSN - 1175-3277
DOI - 10.1007/s40256-020-00437-7
Subject(s) - kexin , lipoprotein , pcsk9 , medicine , cholesterylester transfer protein , proprotein convertase , paraoxonase , lipoprotein(a) , apolipoprotein b , pharmacology , pon1 , pharmacotherapy , coronary artery disease , endocrinology , cholesterol , chemistry , ldl receptor , biochemistry , oxidative stress , genotype , gene
Lipoprotein(a) is a unique form of low-density lipoprotein. It is associated with a high incidence of premature atherosclerotic disease such as coronary artery disease, myocardial infarction, and stroke. Plasma levels of this lipoprotein and its activities are highly variable. This is because of a wide variability in the size of the apolipoprotein A moiety, which is determined by the number of repeats of cysteine-rich domains known as "kringles." Although the exact mechanism of lipoprotein(a)-induced atherogenicity is unknown, the lipoprotein has been found in the arterial walls of atherosclerotic plaques. It has been implicated in the formation of foam cells and lipid deposition in these plaques. Pharmacologic management of elevated levels of lipoprotein(a) with statins, fibrates, or bile acid sequestrants is ineffective. The newer and emerging lipid-lowering agents, such as the second-generation antisense oligonucleotides, cholesteryl ester transfer protein inhibitors, and proprotein convertase subtilisin/kexin type 9 inhibitors offer the most effective pharmacologic therapy.

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